Attachment theory postulates that the establishment of attachment bonds represents an innate, biologically programmed behavior. Its biological function is to enhance the chances of survival in times of danger and need. Accordingly, (almost) all children become attached to survive. However, beyond such basic biological function associated with survival, attachment theory emphasizes the existence of considerable inter-individual differences in attachment quality. These inter-individual differences in attachment quality are usually captured through secure versus insecure – anxious and avoidant – attachment orientations, and are used to predict universal strategies to either draw near, or away, from significant others during situations of personal distress.

Since Bowlby’s pioneering writings on the theory of attachment, attachment researchers have been intrigued by the question how secure versus insecure attachment orientations emerge during human development. The most plausible explanation considers both genetic and social factors, in that, as Jay Belsky puts it nicely in one of his blog posts: “it appears that some children are simply born secure, whereas others are made secure or insecure by, as theory would have it, the quality of rearing they experience“.

The above view that secure versus insecure attachment orientations emerge during development depending on both genetic and social factors was elegantly demonstrated by the seminal work of Weaver and colleagues in rats (original publications: 1999 and 2004). A comprehensive and interactive online summary is available from the University of Utah Genetic Science Learning Center via the website “Lick Your Rats“.

In Weaver and colleagues’ work, the researchers selected rat mothers by naturally occurring inter-individual differences in maternal behavior, quantified by low versus high licking and grooming (LG) and arched-back nursing (ABN). Within this context, a high LG-ABN rat mother would most closely resemble a sensitive / available human mother and thus a rearing environment favoring the emergence of a secure attachment orientation in the offspring. In turn, a low LG-ABN rat mother would most closely resemble an insensitive / unavailable human mother and thus a rearing environment favoring the emergence of an insecure attachment orientation in the offspring.

The researchers then examined adult pups of low and high LG-ABN rat mothers that were either brought up by their own / biological mother, or reared by a foster mother. In so doing, the researchers found that some pups were “born secure” (i.e. adult pups from a high LG-ABN mother reared by a low LG-ABN foster mother resembled adult pups born and reared by a high LG-ABN mother), whilst others “were made secure by the quality of rearing” (i.e. adult pups from a low LG-ABN mother reared by a high LG-ABN foster mother resembled adult pups born and reared by a high LG-ABN mother).

In addition to showing the above patterns based on observing the adult rat pups’ behavior, Weaver and colleagues also provided an underlying biological mechanism reflecting a gene by environment interaction. They found that the influence of the environment on pup development was maintained by non-genomic transmission of individual differences in terms of epigenetic DNA modification. Specifically, they observed that expression of the glucocorticoid receptor as important part of the HPA axis regulating stress was altered in rat pups through DNA methylation, thereby determining how strongly the rat pups responded to stress during adulthood.

Since Weaver and colleagues reported the above findings in rats, some evidence for the same mechanism involving epigenetic modification of the glucocorticoid receptor has been found in humans postmortem (associated with childhood abuse). It therefore appears that both genetic and social factors also play a role in human development. A nice overall summary mentioning the experiments in low versus high LG-ABN rats, and more generally discussing the associated nature versus nurture debate in relation to human development, can be found in this YouTube video (University of Oslo).

According to the above-described theoretical considerations and animal data, we set out to investigate whether we could find evidence for a gene by environment interaction in association with attachment in humans. To this end, we turned to attachment theory and its assumption that inter-individual differences in attachment orientations can be used to predict universal strategies to either draw near, or away, from significant others during situations of personal distress.

To capture the propensity to approach (or avoid) others, we used a biological marker associated with the oxytocin system, namely the oxytocin receptor gene (OXTR). As for the study in rats, we then also assessed the glucocorticoid receptor gene (NR3C1) associated with the HPA stress axis, and particularly the negative feedback loop to end the stress response. In both cases we looked at the degree of gene promoter methylation as a function of attachment security versus insecurity (i.e. attachment avoidance and anxiety), the latter obtained through an attachment self-report questionnaire. To analyze OXTR and NR3C1 promoter methylation, our participants – 109 young healthy adults (56 female) – provided saliva samples.

What we observed was a specific effect for attachment avoidance: the higher our participants scored on attachment avoidance (i.e. high levels of attachment avoidance with concomitantly low levels of attachment anxiety), the more OXTR and NR3C1 promoter methylation was present. Furthermore, we did not find any differentiation between attachment security and anxiety – they both were linked to similar levels of OXTR and NR3C1 promoter methylation. The same was true for a combination of high attachment anxiety and avoidance (fearful-avoidant).

Although these findings are preliminary and need replication and further extension, they tentatively suggest that attachment in humans could also be related to epigenetic DNA modification, particularly in two systems associated with the social regulation of stress. What is interesting is that attachment avoidance appears to be most strongly linked to OXTR and NR3C1 promoter methylation, with attachment avoidance most consistently showing links to diminished social responding and support-seeking in humans.

Caution is advised, however, when interpreting our findings, because they emerged from a correlational study and only reflect epigenetic DNA modification at one time point. We can therefore not establish any causal relationship between OXTR and NR3C1 promoter methylation and attachment (avoidance) in humans as of yet. These and some additional limitations are explicitly mentioned in the corresponding publication (see below).

Despite the currently present limitations, we think that the assessment of gene (promoter) methylation offers a promising new avenue to study gene by environment interactions in the context of human attachment, and hope that this approach may inform future prevention and intervention strategies.